GRIN2A Membrane Protein Introduction

Introduction of GRIN2A

Glutamate receptor ionotropic, NMDA 2A (GRIN2A) is a subunit of the NMDA receptors. This protein in humans is encoded by the GRIN2A gene. It can form di-heteromers or tri-heteromers with the other subunits such as GRIN1, GRIN2B, GRIN2C, GRIN2D, or GRIN3 to generate functional NMDARs. Structurally, GRIN2A has three transmembrane segments and a reentrant pore loop. GRIN2A expression is ubiquitous in the central nervous system (CNS), starting at very low levels around the time of birth, and increasing dramatically during the second postnatal week. During the second postnatal week, GRIN2A replaces GRIN2B as the primary GRIN2 subunit at synaptic sites in the cortex and hippocampus. Through the C-termini of GRIN2A, it can interact with multiple intracellular proteins to mediate multiple physiological functions. However, many of the molecular mechanisms regulating GRIN2A trafficking remain to be elucidated.

Basic Information of GRIN2A
Protein Name Glutamate receptor ionotropic, NMDA 2A
Aliases NMDAR2A, NR2A, hNR2A
Organism Homo sapiens (Human)
UniProt ID Q12879
Transmembrane Times 3
Length (aa) 1,464

Functions of GRIN2A Membrane Protein

GRIN2A proteins are highly expressed in the cortex and hippocampus, and play a critical role in the synaptic function by controlling synaptic plasticity and metaplasticity. However, the exact role of GRIN2A in long-term potentiation and long-term depression is still controversial. Besides, studies in mice lacking the GRIN2A have demonstrated that it is also involved in learning and memory. Moreover, GRIN2A is implicated in different human neurological diseases and disorders, such as cerebral ischemia, seizure disorder, Alzheimer's disease, schizophrenia, Parkinson’s disease, and systemic lupus erythematosus. However, the causality between GRIN2A and these brain diseases has not been determined. Moreover, only a small number of reports have suggested treatment strategies based on GRIN2A or its signaling pathways. The pharmacological potential of this protein remains to be further explored in the future.

GRIN2A Membrane Protein Introduction

Application of GRIN2A Membrane Protein in Literature

  1. Marquardt K., et al. Loss of GluN2A-containing NMDA receptors impairs extra-dimensional set-shifting. Genes Brain & Behavior. 2015, 13(7): 611-617. PubMed ID: 25059550

    This study investigated the contribution of GluN2A subunit to synaptic plasticity and learning in GluN2A knockout, heterozygous, and wild-type mice.

  2. Balsara R.D., et al. Probing NMDA receptor GluN2A and GluN2B subunit expression and distribution in cortical neurons. Neuropharmacology. 2014, 79(4): 542-549. PubMed ID: 24440368

    This article investigated the distribution of GluN2A and GluN2B subunits from L5 neurons of wild-type and GluN2A-deficient mice, using focal laser scanning photostimulation of caged glutamate, slice electrophysiology, and small peptide antagonists.

  3. Hackos D., et al. Positive allosteric modulators of GluN2A-containing NMDARs with distinct modes of action and impacts on circuit function. Neuron. 2016, 89(5): 983-999. PubMed ID: 26875626

    This article described the identification of positive allosteric modulators (PAMs) of NMDARs with selectivity for GluN2A-containing receptors.

  4. Volkmann R.A., et al. MPX-004 and MPX-007: new pharmacological tools to study the physiology of NMDA receptors containing the GluN2A subunit. Plos One. 2016, 110(3): 288a-288a. PubMed ID: 26829109

    This article reported a group of pyrazine-containing GluN2A antagonists, such as MPX-004 and MPX-007. The selectivity and potency were studied. The results showed these antagonists were highly selective pharmacological probes to explore the physiology and their therapeutic potential.

  5. Holehonnur R., et al. Increasing the GluN2A/GluN2B ratio in neurons of the mouse basal and lateral amygdala inhibits the modification of an existing fear memory trace. Journal of Neuroscience the Official Journal of the Society for Neuroscience. 2016, 36(36): 9490. PubMed ID: 27605622

    This article reported that auditory fear memories created with 10 tone-shock pairings were resistant to retrieval-dependent memory destabilization and were associated with an increase in the synaptic GluN2A/GluN2B ratio in neurons of the basal and lateral amygdala (BLA) compared with weaker fear memories created via one or three tone-shock pairings.

GRIN2A Preparation Options

Membrane proteins like GRIN2A are required to be solubilized and stabilized in an amphiphilic environment for isolation as well as subsequent structural and functional studies. As an undisputed leader in membrane protein production, Creative Biolabs is proud to recommend our powerful Magic™ membrane protein production platform to obtain your target protein in a variety of formats. Specific strategies and methods can be customized based on your project demands. Our experts will give professional advice on the selection of optimal formats. Aided by our versatile Magic™ anti-membrane protein antibody discovery platform, we also provide customized anti-GRIN2A antibody development services.

Moreover, Creative Biolabs is specialized in the membrane protein characterization and antibody discovery targeting these membrane protein antigens. Contact us to get full advice from our experts on your membrane protein studies.

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